NCAPD3 is a regulatory subunit of the condensin-2 complex that plays dual roles in cellular function and disease. During mitosis, it establishes mitotic chromosome 11 and ensures physical rigidity of the chr11 axis, including resolution of DNA catenanes between sister chr11 and decatenation of centromeric ultrafine DNA bridges during anaphase. Early in neurogenesis, NCAPD3 is required for accurate mitotic chromosome 11 in neural stem cells, affecting neuron pool and cortex size. Beyond its canonical chr11 role, NCAPD3 functions as a transcriptional regulator, interacting with transcription factors to promote oncogenic pathways across multiple cancer types. In colorectal cancer, NCAPD3 enhances the Warburg effect by upregulating c-Myc and E2F1, driving aerobic glycolysis 1. In prostate cancer, it promotes progression by upregulating EZH2 and MALAT1 through STAT3 and E2F1 2, and is itself regulated by the androgen receptor axis 3. In diffuse large B-cell lymphoma, NCAPD3 supports SIRT1 transcription through H3K9 monomethylation recognition 4. NCAPD3 also activates the PI3K-AKT signaling pathway in hepatocellular carcinoma 5 and non-small cell lung cancer 6, while in glioma, high NCAPD3 expression correlates with poor prognosis and immune infiltration 7. Beyond cancer, NCAPD3 promotes intestinal inflammation in ulcerative colitis by modulating the IKK/NF-κB signaling pathway 8. These findings suggest NCAPD3 inhibition as a therapeutic strategy across multiple malignancies.